Essay on Endothelium in Health and Disease

2. Explain the effect that the change in blood vessel length had on flow rate. How well did the results compare with your prediction?

When substances like Acetylcholine (Ach) and norepinephrine which are small- molecular neurotransmitters are released into the body they bind to receptors on tissue or neurons through our ANS and PNS system. Ach is released by many PNS neurons and some CNS neurons. In the PNS Ach is an excitatory neurotransmitter at some synapses, such as the neuromuscular junction where it binds to ionotropic receptors which open cation channels. Ach can also be an inhibitory neurotransmitter at other synapses, where it binds to metabotropic receptors while opening potassium channels. The enzyme acetylcholinesterase (AchE) inactivates Ach by splitting into acetate and choline fragments. Norepinephrine (NE) is a biogenic amine; most biogenic amines may cause

AChE is found in red blood cells, cholinergic fibres and muscle (motor end-plate), existing as mainly membrane bound (Rang & Dale, 2007). It is highly specific for the neurotransmitter acetylcholine (ACh) and its principle role is termination of impulse

This will be done by anesthetizing the crayfish in ice, and dissecting it until only the cephalothorax remains with the heart visibly beating. This will allow for easy addition of our select neurotransmitters: acetylcholine (ACh) and dopamine (DA). Two separate experiments will be performed. One will test for the presence of cholinergic receptors and the other will test for the presence of dopaminergic receptors. In order to test for cholinergic receptors, a multi-tiered experiment will be done. One crayfish will first be exposed to ACh only and will be followed by another test with atropine. This will give information on which receptor might be present. To test for dopaminergic receptors, simply adding dopamine to the heart will provide an answer to whether these receptors are present.

Acetylcholine is found at the peripheral nervous system and synapses in the central nervous system within the human body. Acetylcholine is an excitatory neurotransmitter that conducts electrical impulses, allowing nerve cells to communicate with muscle cells and generate muscle contractions. However, acetylcholine produces an inhibitory effect in cardiac muscle. (Waymire, 1997) Therefore, once the Daphnia are exposed to acetylcholine, their heart rate is expected to decline. In contrast, epinephrine, also known as adrenaline, is a hormone which binds to the beta adrenergic receptors in the heart leading to increases in the firing rate of the pacemaker cells. (Meyers, 2011) Therefore, the Daphnia’s heart rate is expected to increase with exposure to

I now know that the hypotension is caused by vasodilatation because the sympathetic nerves that control tone are blocked. Peripheral

What are the clues that helped the paramedic determine why the nitroglycerin did not alleviate the man’s angina?

The muscarinic AChRs occur primarily in the CNS, and are part of a large family of G-protein-coupled receptors (‘G proteins’), which use an intracellular secondary messenger system involving an increase of intracellular calcium to transmit signals inside cells. Binding of acetylcholine to a muscarinic AChR causes a conformational change in the receptor that is responsible for its association with and activation of an intracellular G protein, the latter converting GTP to GDP in order to become activated and dissociate from the receptor. The activated G

In order to understand NO’s neurobiological roles, some of NO’s biochemistry and physiology must be discussed. NO’s radical structure, fleeting half-life, and rapid diffusibility make it an ideal neurotransmitter, albeit an unconventional one. In the peripheral vascular blood supply, acetylcholine or bradykinin act on endothelial cells in the vessels which causes a release of endothelium-derived relaxation factor (EDRF) which has been verified to be NO (Snyder;1992). Acetylcholine or bradykinin causes an increase in the intracellular Ca2+ concentration through the action of inositol triphosphate; the increased intracellular Ca+ binds the calmodulin site in NOS and stimulates the synthesis of NO which rapidly diffuses away from its site of synthesis to the tunica muscularis of blood vessels causing vasodilation (Murray;1993). In this manner, NO is a sort of second neurotransmitter potentiating the effects of acetylcholine or bradykinin on the muscular layer of blood vessels. In this system, NOS is located in the endothelial cells; however, in the cerebral arteries, NOS is located in the nerve plexus themselves in the outer layer of cerebral arteries, and the cell bodies of these neurons lie in the sphenopalatine

Molecular signalling of these receptors activates a wide range of actions. Generally, these actions are meant to make cell membranes less excitable and also initiate suppression of actions of pathways that control blood pressure, breathing and heart rate. Morphine receptors may include Mu receptors found in the thalamus and the brainstem. Activation of these receptors translates into pain relief, euphoria and sedation. Another class of receptors is the kappa receptor found in the limbic system, spinal cord, and the brain stem. Activation of this receptors also causes sedation and pain relief. The delta receptor, on the other hand, is abundant in the brain, spinal cord, and digestive tract. Activation of this receptor results in both analgesic and antidepressant effects (McGavock, 2011). Despite morphine being relatively selective for the mu receptor, it interacts with other opioid receptors when at high

It has been proposed that pulmonary vasoconstriction occurs as an early event of PAH, and is due to abnormal potassium channel expression and endothelial dysfunction. The endothelium is a key regulator of vascular tone and subsequently blood pressure. Endothelial dysfunction results in chronic release of vasoconstrictive agents such as endothelin-1 (ET-1) and impaired production of vasodilatory agents such as nitric oxide (NO) and prostacyclin(2). The effects of the sustained increase in ET-1 seen in PAH makes this molecule a major pharmacological

Selective α1 antagonists work on the post-synaptic α1 adrenoreceptors predominantly found in vascular smooth muscle. These receptors are normally bound by norepinephrine or epinephrine to mediate regulation of the cardiovascular system by the sympathetic nervous system. As can be seen in Figure 1, these receptors are bound to Gq-proteins which have two signal transduction pathways. One of the pathways forms IP3 (Inositol triphosphate) which then stimulates the release of Calcium from the sarcoplasmic reticulum in a cardiac monocyte (Klabunde, R.E., 2013). The release of calcium then stimulates contraction in the heart. By selectively inhibiting these adrenoceptors, vasodilation occurs which in turn causes a decrease in arterial pressure (Rang and Dale).

[Q3] The adrenergic receptors that are stimulated to improve consciousness include both alpha and beta receptors. This is due to epinephrine being a vasoactive adrenergic, and the affect on both receptors results in cardiac failure support. The alpha-1 receptor acts on the nerve

The aim of the experiment was to investigate the effect of three antagonists; atropine, tubocurarine, and mepyramine on the agonist acetylcholine using isolated tissue from guinea pig ileum that has been bathed in physiological salt solution. In the guinea-pig ileum, which is a smooth muscle, acetylcholine causes contraction by binding to the muscarinic receptors (Unno, et al., 2005). Acetylcholine is a neurotransmitter that acts in the central nervous system and is an agonist to two main types of receptors called muscarinic and nicotinic. The muscarinic receptors are G-protein-coupled-receptors that commonly produce a parasympathetic response when bound to acetylcholine, however Nicotinic are ligand-gated receptors that produce both a sympathetic

To modulate arterial blood pressure, which is a key factor in successful delivery of blood to tissues, the smooth muscles of the aorta and other arteries will either vasoconstrict or vasodilate in response to amount of blood flow based on nervous system controls (9). This mechanical adaptation is effective, because the blood flow is inversely proportional to fourth power of radius change in vessel and a slight change in vessel diameter will easily accommodate pressure difference in cardiac cycles. The blood flows in a pulsatile wave manner – a dicrotic notch corresponding to fall back of blood toward aortic valve is observed in aortic pressure immediately following the aortic valve closing – the degree of stress, whether it be a shear stress or an outward stress, is not uniform throughout the cardiac cycle (1, 11, 18). Adequate vasoconstriction or vasodilation can match vessel stress with the changing blood flow, and a laminar blood flow can be maintained despite of pulsatile blood flow especially in abdominal aorta, which has less natural turbulent flow that ascending and thoracic aorta may experience due to aortic arch